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Renal Control of Acid-Base Balance Flashcards

1
Q

Why must pH stay at 7.4?

A
  • some AA have net positive charge or net negative charge at this ph
  • any changes will impact electrostatic charge needed for proper protein folding, alters protein -protein interaction, drug binding/ability to enter cells, etc
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2
Q

Which metabolic acid sources are used for volatile purposes?

- where in body

A

Glucose + O2 -> H+ + HCO3-

Fat + O2 -> H+ + HCO3-

in Lungs (24,000 mEq/ day)

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3
Q

Which metabolic acid sources are used for fixed (nonvolatile) purposes?
- where in body

A

Glucose (anaerobic) -> H+ + lactate

Cysteine + O2 -> H+ + sulfate

Phosphoprotein + O2-> H+ + phosphate

kidneys
(50 mEq/day)

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4
Q

Meaning of Pk

A

pH at which this buffer, acting as “H+ sponge” has sopped up half of the H+ it can hold

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5
Q

Ph of gastric HCl

A

0.8

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6
Q

HCO3-/ H2CO3

  • name buffer system
  • pK value
  • Reaction equation
A

bicarbonate

6.1

H+ + HCO3- <=> H2O + CO2

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7
Q

Hb-/ HHb

  • name buffer system
  • pK value
  • Reaction equation
A

hemoglobin

7.3

HHb <=> H+ + Hb-

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8
Q

HPO4/ H2PO4

  • name buffer system
  • pK value
  • Reaction equation
A

Phosphate

6.8

H2PO4 <=> H + HPO4-

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9
Q

Pr-/ HPr

  • name buffer system
  • pK value
  • Reaction equation
A

plasma proteins

6.7

HPr <=> H+ + Pr-

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10
Q

Four buffer pairs in body buffer system

- what is their rates

A

1) HCO3/ H2CO3
2) Hb-/ HHb
3) HPO4/ H2PO4
4) Pr-/ HPr

ALL instantaneous

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11
Q

Organs in Body Buffer System (4)

- list mechanism

A

1) Lungs
- regulates retention/ elimination of CO2 and H2CO3
2) Ionic Shifts
- exchange of intracellular K and Na for hydrogen
3) Kidneys
- bicarbonate reabsorption/regeneration, ammonia formation, phosphate buffering
4) Bone
- exchange of calcium, phosphate, release of carbonate

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12
Q

Buffering of Hydrogen Ion by Plasma Proteins and Hemoglobin

  • how does H+ enter body for buffering?
  • transport
A

CO2 enter tissues

3 ways of CO2 breakdown in RBC:

a) CO2 dissolved
b) CO2 + H2O <=> H2CO3 <=> HCO3- + H+
c) CO2 + Protein -NH2 <=> Protein + H+

HCO3- + H+
- will use HCO3-/Cl- transport to bring Cl- in , HCO3- out of RBC

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13
Q

Volume of K in ICF? ECF

A 
ICF= 140 mM k+
ECF= 4.0 mM K+
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14
Q

If ECF is in acidemia, what will happen in ICF?

A

ICF takes in H+
= low ECF pH ( <7.35)
= high H+, buffered by raising ECF K+

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15
Q

If ECF is in alkalemia, what will happen in ICF?

A

ICF donates H+
= high ECF pH (>7.45)
= low H, buffered by lowering ECF K

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16
Q

Henderson-Hasselbalch Equation

- which part of equation is controlled by kidneys? lungs?

A

ph= 6.1 + Log [HCO3-]/ [H2CO3]

or

ph= 6.1 + Log [HCO3-]/ (0.03 x PCO2)

[HCO3-]= controlled by kidneys, slow with large capacity

[H2CO3]= controlled by lungs, fast with limited capacity

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17
Q

Ventilatory Rate effect on pH

- hyperventilation? hypoventilation?

A

Hyperventilation= less CO2= less H2Co3= less H= high pH

Hypoventilation= more CO2= more H2Co3= more H= low pH

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18
Q

Renal Reabsorption of Bicarbonate (%)

  • PT
  • Thick LOH
  • CD
A

in Glomerulus : 4320 mEq/ Day

  • PT: 85% , 3672 mEq/ day
  • Thick LOH: 10%, 432 mEq/day
  • CD: 4.9%, 215 mEq/day
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19
Q

Detailed Reabsorption of filtered bicarbonate by Proximal Tubule

  • transports on apical side
  • transports on basolateral side
A

Apical side

  • Na/H exchange ( Na in , H+ out of tubular fluid)
  • H ATPase
  • Bicarbonate -> H2O + Co2 enter cell via carbonic anahydrase

Basolateral side

  • Na/K Atpas
  • Na/ HCo3- co transport (out)
  • HCO3-/ Cl- ( HCO3 out into blood)
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20
Q

What factors increase H+ secretion?

  • Primary (2) / location
  • Secondary (5)/ location
A

Primary (entire nephron)

1) decrease plasma HCO3- (decrease pH)
2) Increase in partial pressure at arterial carbon dioxide

Secondary (all are in PT except #4 is CD)

1) increased in HCO3- filtered load
2) decrease ECF volume
3) increase Ang II
4) increase aldosterone
5) Hypokalemia

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21
Q

What increased during hypokalemia?

why?
- what transporters are involved?

A

ammonia genesis and net acid secretion increased

  • intracellular acidifcation
  • hormones upregulates ammoniagenesis genes to increase NH4+ excretion and decrease K+ secretion
  • renal glutamin transporter SN1
  • mitochondrial glutaminase (GA)
  • glutamate dehydrogenase (GDH)
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22
Q

What factors decrease H+ secretion?

  • Primary (2) / location
  • Secondary (5)/ location
  • when is hyperkalemia relevant
A

Primary (entire nephron)

1) increase plasma HCO3- (increase pH)
2) decrease in partial pressure at arterial carbon dioxide

Secondary (all are in PT except #3 is CD)

1) decreased in HCO3- filtered load
2) increase ECF volume
3) decrease aldosterone
4) Hyperkalemia
- during type IV renal tubular acidosis

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23
Q

Phosphate buffering of secreted hydrogen ions

  • what transports are on apical side?
  • what transports are on basolateral side?
  • what is pathway for Na
A
  • regenerates the plasma HCO3- that had been “consumed” elsewhere when NaH2PO4 lost an H= in acid body
  • H+ into urine

Basolater side

  • Na/K ATPase
  • passive diffusion for HCO3 and CO2

Apical side
- Na/H exchange ( H out into tubular lumen)

NaHPo4- (from tubular lumen) -> NaHPo4 + H+ -> NaH2PO4 -> carries H into the lumen

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24
Q

How ammonia in nephron generate new Bicarbonate

  • in proximal tubule
  • in collecting duct

significance

A

PT
- Glutamine in lumen-> breakdown to ammonia (x2) -> NH3 goes out into tubular fluid -> combine with H+ -> form NH4

-NH3 reabsorbs in tubular fluid

CD
- CO2 + H2O -> H2CO3 via CA-> breaks down into HCO3 + H

HCO3 -> reabsorbs into blood
H+ ->enters tubular fluid into CD

H+ combines with NH3 to become NH4 and excreted into urine

  • uses Na/K/2CL transporter
    NH4 replaces K in this transporter
  • diffuses into CD where it is ion trapped
25
Reabsorption and secretion of bicarbonate in Alpha intercalated cells - transporter on apical side - transporter on basolateral side - significance
- secretes H - Reabsorbs HCO3- apical side - K/H ATPase ( K in ) - H ATPase ( H out) basolateral membrane - HCO3/ Cl- antiporter (HCO3 in) - "new" bicarbonate is generated during process of urinary acidification when secreted H+ is buffered by NH3-> NH4+, phosphate for excretion while bicarbonate is reabsorbed
26
Reabsorption and secretion of bicarbonate in Beta intercalated cells - transporter on apical side - transporter on basolateral side
- reabsorbs H+ - secretes HCO3- Apical Side - HCO3/ Cl- antiporter (HCO3 in tubular fluid) Basal Side - H+ Atpase ( H into blood)
27
Net Acid Excretion Equaion | - what must it equal?
NA= (U(nh4) x V) + (U (Ta) x V) - (U (HCO3) x V) - NAE must equal nonvolatile acid production each day in order to maintain acid-base balance
28
Titratable Acids
salts of primarily phosphate, sometimes creatinine | ~ 1/3 NAE
29
Ammonium ( Nh4+)
synthesis and secretion is responsible for ~2/3 NAE -body can easily make as much as needed
30
Why is ammonium is not measured as about of titratable acidity?
high pK of ammonium means no H is removed from NH4 during titration to a ph of 7.4
31
Normal Values of Acid- Base Disturbances - ph - H+ - Pco2 - HCO3-
ph= 7.4 H+= 40 mEq/L PCO2= 40 mmHg HCo3-= 24 mEq/L
32
Respiratory Acidosis - ph - H+ - Pco2 - HCO3-
- decrease ph - increase H+ - increase Pco2 - increase HCO3-
33
Respiratory Alkalosis - ph - H+ - Pco2 - HCO3-
- increase ph - decrease H+ - decrease Pco2 - decrease HCO3-
34
Metabolic Acidosis - ph - H+ - Pco2 - HCO3-
- decrease ph - increase H+ - decrease Pco2 - decrease HCO3-
35
Metabolic alkalosis - ph - H+ - Pco2 - HCO3-
- increase ph - decrease H+ - increase Pco2 - increase HCO3-
36
Metabolic Acidosis with compensation and correction | - pathway
Renal low serum ph-> increased acid titration -> increase ammonium and H2PO4-> increase acid excretion in urine-> increase bicarbonate regeneration -> increase serum ph Respiratory low serum ph-> hyperventilation-> decrease PCo2-> decrease CO2 + H2O-> decrease H2Co3-> decrease H
37
Normal Anion Gap
8-16 mEq/L
38
Causes of Metabolic Acidosis - High Anion Gap (9) - Non- Anion Gap (7)
High Anion Gap (MUDPILERS) - Methanol - Uremia - DKA/ Alcoholic Ketoacidosis - Paraldehyde ( obsolete sedative-hypnotic) - Isoniazid (used to treat tuberculosis) - Lactic Acidosis - EtOH/ Ethylene Glycol - Rhabdo/ Renal failure - Salicylates Non-Anion Gap (HARDUPS) - Hyperalimentation - Acetazolamide - Renal Tubular Acidosis - Diarrhea - Uretero-Pelvic Shunt - Post-hypocapnia - Spironolactone
39
Causes of Metabolic Acidosis (3)
1) Excessive production or ingestion of fixed H+ 2) loss of HCO3- - Type 2 renal tubular acidosis ( renal loss of HCO3-) 3) Inability to excrete fixed H - Type 1 renal tubular acidosis ( decrease excretion of H as titratable acid and NH4) - Type 4 renal tubular acidosis ( hyperaldosteronism)
40
Type 1 Renal Tubular Acidosis - location - acidosis? - potassium - pathophysiology - what does it impair
- distal tubules - severe acidosis, normal anion gap - hypokalemia - failure of H+ secretion by alpha intercalated cells - impair acid-base homeostasis and phosphate/ammonia buffer - urinary stone formation due to hypercalciuria - bone demineralization
41
Type 2 Renal Tubular Acidosis - location - acidosis? - potassium - pathophysiology
- Proximal Tubules - acidosis - hypokalemia - failed HCO3- reabsorption from urine by proximal tubular cells
42
Type 4 Renal Tubular Acidosis - location - acidosis? - potassium - pathophysiology
- adrenal - mild acidosis with normal anion gap - hyperkalemia - deficiency/ resistance to aldosterone bc psuedomypoaldosteronism or drug - low aldosterone/ failure to respond to it - decrease NH3 synthesis by PT - ACE inhibitors , spironolactone can cause this impair acid-base homeostasis
43
Metabolic Acidosis Symptoms - mild - with ph <7.10
mild acidosis- asymptomatic with ph< 7.10 ( or higher if rapidly developed) - nausea, vomiting, malaise see long deep breaths at normal rate (respiratory compensation) without dyspnea
44
Metabolic Alkalosis with Compensation and Correction | - pathway
Renal - high serum ph-> decrease tubular reabsorption of bicarbonate -> increase bicarbonate excretion in urine -> low serum ph - high serum ph-> decrease acid titration -> decrease ammonium and HPO4-> decrease bicarbonate regeneration -> decrease acid excretion in urine -> low serum pH Respiratory - high serum ph-> hypoventilation -> increase PCO2-> increase CO2 + H2O-> increase H2Co3-> increase H+ -> low serum ph
45
Causes of Metabolic Alkalosis (8)
- Contraction - Licorice - Endo ( Conn, Cushing, Bartter) - Vomiting - Excess Alkali - Refeeding Alkalosis - Post-hypercapnia - Diuretics
46
Causes of Metabolic Alkalosis
1) Loss of H (vomiting, hyperaldosteronism) 2) Gain of HCO3 (ingestion of NaHCo3) 3) Volume contraction alkalosis (loop or thiazide diuretic)
47
Metabolic Alkalosis Symptoms - mild - more severe
Mild: symptoms of underlying disorder severe: increased binding of CA2+=> hypocalcemia - headache, lethargy, neuromuscular excitability, - delirium, tetany, seizures - angina symptoms, arrhytias, weakness
48
Respiratory Acidosis with compensation | - pathway
decrease ventilation-> increase blood PCo2-> increase bicarbonate-> low serum ph -> renal compensation-> increased acid titration -> increase ammonium and HPO4--> increase acid excretion in urine-> increase bicarbonate regeneration-> increase serum pH
49
Causes of Respiratory Acidosis - acute (4) - chronic (2)
``` Acute CANS - CNS depression - Airway obstruction - Neuromuscular disorders - Sever Pneumonia, embolism, edema ``` Chronic - COPD ( chronic obstructive pulmonary disease) - anything chronic that leads to impaired ventilation
50
Causes of Respiratory Acidosis (4)
1) inhibition of medullary respiratory center - opiates, barbiturates 2) disorders of respiratory muscles - ALS - MS 3) airway obstruction - aspiration - obstructive sleep apnea - laryngospasm 4) disorders of gas exchange - COPD - Pneumonia - pulmonary edema
51
Respiratory Acidosis Symptoms - acute - slowly developing, stable
acute - headache, confusion, anxiety, drowsiness, stupor, tremors, convulsion, possible coma (CO2, narcosis) Slowly developing, Stable (as in COPD) - may be well tolerated - memory loss, sleep disturbances, excessive daytime sleepiness, and personality changes - gait disturbance, tremor, blunted deep tendon reflexes, myoclonic jerks, asterixis, papilledema
52
Respiratory Alkalosis with Compensation | - pathway
increased ventilation-> low blood PCo2-> decrease H+ and H2CO3-> increase serum pH-> renal compensation-> decreased acid titration-> decrease NH4 and HPO4-> decrease acid excretion in urine-> decrease bicarbonate regeneration -> low serum ph
53
Causes of Respiratory Alkalosis (6)
CHAMPS - CNS Disease - Hypoxia - Anxiety - Mechanical Ventilators - Progesterone - Salicylates/ Sepsis
54
Causes of Respiratory Alkalosis (3)
1) stimulation of medullary respiratory center - neurological disorder 2) Hypoxemia - high altitude - pneumonia - pulmonary embolism - severe anemia 3) Mechanical Ventilation
55
Respiratory Alkalosis Symptoms - acute - chronic
Acute - light headedness - confusion - peripheral and circumoral paresthesias - cramps - syncope - tachypnea/ hyperpnea - carpopedal spasm due to decrease hypocalcemia Chronic - asymptomatic
56
Metabolic Acidosis Equations
PaCo2= 40- (1.2 x (24-HCO3-) PaCo2= (1.5 x HCO3) + 8 +/- 2
57
Metabolic Alkalosis Equation
PaCo2= 40 + (0.7 x HCO3- 24) must be less than 20
58
Respiratory Acidosis Equations
Acute HCO3- = 24 + (0.1 X (PaCo2-40)) Chronic HCO3-= 24 + (0.4 X (PaCo2-40))
59
Respiratory Alkalosis Equations
Acute HCO3- = 24 - (0.2 X (40- PaCo2)) Chronic HCO3-= 24 - (0.5 X (40-PaCo2)) Range +/- 2

Renal Final (7 decks)

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